Scovino Aline Miranda, Dahab Elizabeth Chen, Diniz-Lima Israel, de Senna Silveira Etiele, Barroso Shana Priscila Coutinho, Cardoso Karina Martins, Nico Dirlei, Makhoul Gustavo José, da Silva-Junior Elias Barbosa, Freire-de-Lima Celio Geraldo, Freire-de-Lima Leonardo, Fonseca Leonardo Marques da, Valente Natalia, Nacife Valeria, Machado Ana, Araújo Mia, Vieira Gustavo Fioravanti, Pauvolid-Corrêa Alex, Siqueira Marilda, Morrot Alexandre
Instituto de Microbiologia, Universidade Federal do Rio de Janeiro, Rio de Janeiro 21941-902, Brazil.
Laboratório de Imunoparasitologia, Fundação Oswaldo Cruz (Fiocruz), Rio de Janeiro 21040-360, Brazil.
Microorganisms. 2024 Apr 2;12(4):720. doi: 10.3390/microorganisms12040720.
The SARS-CoV-2 P.1 variant, responsible for an outbreak in Manaus, Brazil, is distinguished by 12 amino acid differences in the S protein, potentially increasing its ACE-2 affinity and immune evasion capability. We investigated the innate immune response of this variant compared to the original B.1 strain, particularly concerning cytokine production. Blood samples from three severe COVID-19 patients were analyzed post-infection with both strains. Results showed no significant difference in cytokine production of mononuclear cells and neutrophils for either variant. While B.1 had higher cytopathogenicity, neither showed viral replication in mononuclear cells. Structural analyses of the S protein highlighted physicochemical variations, which might be linked to the differences in infectivity between the strains. Our studies point to the increased infectivity of P.1 could stem from altered immunogenicity and receptor-binding affinity.
导致巴西玛瑙斯疫情爆发的新冠病毒P.1变体，其刺突蛋白存在12个氨基酸差异，这可能会增加其对血管紧张素转换酶2（ACE-2）的亲和力和免疫逃逸能力。我们研究了该变体与原始B.1毒株相比的先天免疫反应，特别是关于细胞因子的产生。对三名重症新冠肺炎患者感染这两种毒株后的血液样本进行了分析。结果显示，两种变体的单核细胞和中性粒细胞产生细胞因子的情况均无显著差异。虽然B.1具有更高的细胞致病性，但两种变体在单核细胞中均未显示病毒复制。刺突蛋白的结构分析突出了物理化学变化，这可能与毒株之间的感染性差异有关。我们的研究表明，P.1感染性增加可能源于免疫原性和受体结合亲和力的改变。
